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MLL2, but not MLL1, plays a major role to sustain leukemia survival [array]

ABSTRACT: The MLL1 histone methyltransferase gene undergoes many distinct chromosomal rearrangements to yield poor-prognosis leukemia. The remaining wild-type allele is most commonly, but not always, retained. To what extent the wild-type allele contributes to leukemogenesis is unclear. Here we show using rigorous, independent animal models that endogenous MLL1 is dispensable for MLL-rearranged leukemia. Potential redundancy was addressed by co-deleting the closest paralog, Mll2. Surprisingly, Mll2 deletion alone had a significant impact on survival of MLL-AF9-transformed cells and additional Mll1 loss further reduced viability and proliferation. We show that MLL1/MLL2 collaboration is not through redundancy but regulation of distinct pathways. These findings highlight the relevance of MLL2 as a drug target in MLL-rearranged leukemia and suggest its broader significance in AML. We used microarray to investigate the effect of Mll1 deletion on gene expression in LSC-enriched MLL-AF9 leukemia cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE93621 | GEO | 2017/01/20

SECONDARY ACCESSION(S): PRJNA362638

REPOSITORIES: GEO

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MLL2, but not MLL1, plays a major role to sustain leukemia survival [RNA-seq]

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MLL2, but not MLL1, plays a major role to sustain leukemia survival

Project description:MLL2, but not MLL1, plays a major role to sustain leukemia survival

| PRJNA362633 | ENA

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Regulation of transcription by MLL2 complex and MLL complexes-associated protein AKAP95

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